ArticleJournal of carcinogenesis & mutagenesis
Regulation of Apoptosis by HER2 in Breast Cancer.
Article in Journal of carcinogenesis & mutagenesis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 76 citations in OpenAlex.
- A comprehensive review on apoptotic miRNAs and antagomiRs in breast cancer: Enhancing radio sensitization.Genes & diseases · 2026Review
- Interpretable deep neural network identifies robust biomarkers for diseases with mechanistic insights from omics data.Briefings in bioinformatics · 2026Article
- Renovascular disease induces functionally relevant, locus-specific alterations to DNA methylation and hydroxymethylation in swine scattered tubular-like cells.American journal of physiology. Renal physiology · 2026Article
- Review
- Review
- Expression of Survivin and HER-2 as Independent Predictive Factors for Treatment Response in Locally Advanced Breast Cancer: A Prospective Cohort Study.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Antibody-drug conjugates in gynecologic malignancies: breakthroughs, challenges, and future directions.Frontiers in immunology · 2026Review
- Article
- Discovery of natural scaffolds as HER2 inhibitors for breast cancer: virtual screening, molecular dynamics, and biological characterization with selectivity profiling.Scientific reports · 2025Article
- Molecular landscape of HER2-mutated non-small cell lung cancer in Northeastern Brazil: Clinical, histopathological, and genomic insights.Oncotarget · 2025Article
- Cardiac Toxicity Under Concurrent Administration of Trastuzumab (Anti-HER2 Therapy) and Radiotherapy: Systematic Review and Meta-Analysis.Health science reports · 2025Review
- Trastuzumab Potentiates Antitumor Activity of Thiopyrano[2,3-Molecules (Basel, Switzerland) · 2024Article
- Cytobiological Alterations Induced by Celecoxib as an Anticancer Agent for Breast and Metastatic Breast Cancer.Advanced pharmaceutical bulletin · 2024Review
- Extracellular Vesicles in Breast Cancer: From Intercellular Communication to Therapeutic Opportunities.Pharmaceutics · 2024Review
- Targeting solid tumor antigens with chimeric receptors: cancer biology meets synthetic immunology.Trends in cancer · 2024Review
- Evaluation of cleaved caspase-3 and Ki-67 index on diagnostic biopsy in response to neoadjuvant chemotherapy in the context of post-treatment tumour ypT stage, ypN stage, grade, and molecular subtype.Przeglad menopauzalny = Menopause review · 2024Article
- Dual-Targeted Therapy in HER2-Overexpressing Breast Cancer with Trastuzumab and Novel Cholesterol-Based Nioplexes Silencing Mcl-1.Pharmaceutics · 2023Article
- Development of High-Loading Trastuzumab PLGA Nanoparticles: A Powerful Tool Against HER2 Positive Breast Cancer Cells.International journal of nanomedicine · 2023Article
- Development of an adverse outcome pathway network for breast cancer: a comprehensive representation of the pathogenesis, complexity and diversity of the disease.Archives of toxicology · 2022Review
- Resistance to Trastuzumab.Cancers · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HER2 is a trans-membrane receptor tyrosine kinase that activates multiple growth-promoting signaling pathways including PI3K-AKT and Ras-MAPK. Dysregulation of HER2 is a frequent occurrence in breast cancer that is associated with poor patient outcomes. A primary function of HER2 is suppressing apoptosis to enhance cell survival giving rise to uncontrolled proliferation and tumor growth. There has been much investigation into the mechanisms by which apoptosis is suppressed by HER2 in hopes of finding clinical targets for HER2-positive breast cancers as these cancers often become resistant to therapies that directly target HER2. Several apoptotic mechanisms have been shown to be deregulated in HER2-overexpressing cells with examples in both the intrinsic and extrinsic apoptotic pathways. HER2-mediated activation of PI3K-AKT signaling is required for many of the mechanisms HER2 uses to suppress apoptosis. HER2 overexpression is correlated with increases in anti-apoptotic Bcl-2 proteins including Bcl-2, Bcl-xL, and Mcl-1. HER2 also suppresses p53-mediated apoptosis by upregulation of MDM2 by activation of AKT. In addition, survivin expression is often increased with HER2 overexpression leading to inhibition of caspase activation. There is also recent evidence to suggest HER2 can directly influence apoptosis by translocation to the mitochondria to inhibit cytochrome
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.